blocking androgen receptor makes things worse?

[baldinglikeamofo]

"It is generally known, at least in males, that extended AR blockade leads to AR mutation, and that the mutated receptor attains the capability to be activated by other substances such as various steroidal metabolites and even progestins and estrogens, insulin-like growth factor, epidermal growth factor and keratinocyte growth factor and neuroendocrine transmitters such as serotonin."


do you guys believe this stuff or is the site I got this from just an ad for fluridil?



http://www.stophairlossnow.com/Products/Fluridil.htm

 

[baldinglikeamofo]

OMG I think its right.

Heres an article why androgen blockade stops working for prostate cancer:


"hey found over-production of these outlaw variants in prostate cancer cells taken from patients whose disease had become resistant to androgen deprivation therapy"

http://www.psa-rising.com/mednews/adt/6 ... pkins.html



so taking cb-03-01 might be a mistake

 

[baldinglikeamofo]

androgen blockage might be the very reason RU works only temporarily for alot of people and why it never made it to the market


lakota, i found what screwed you.

 

[blaze]

first of all what screwed lakota?

second of all AR mutation has only been reported in prostate cancer. which is cancer.

 

[Bryan]

If blocking androgen receptors makes things worse, how does one explain Hamilton's often quoted finding that castration can have its beneficial effect on scalp hair for as long as 20-30 years, and quite possibly even longer? While the sharp curtailment of androgen production (castration) isn't exactly the same thing as androgen receptor blockade, it's certainly in the same general neighborhood. You need to explain that, if you're going to use something that happens with prostate cancer cells as an argument not to use antiandrogens to protect scalp hair.

 

[baldinglikeamofo]

castration totally deprives the body of androgens, so even if the receptors did morph it wouldnt matter, because there are no androgens to interact with it.

 

[blaze]

castration doesnt totally deprive the body of androgens. Just reduces it heavily.

Castrates have roughly the same amount of DHT as finasteride users. But they also have MUCH less Test. But they still have androgens none the less.

 

[Bryan]

Castration decreases serum testosterone by about 90% to 95%, depending on which study you believe. As the poster above mentioned, it also reduces serum DHT by about the same amount that finasteride does, according to one study.

So I ask the question again to the original poster: why doesn't castration cause androgen receptors in the body (including hair follicles) to mutate, so that they become sensitive to substances other than just androgens? And yet Hamilton found that castration can work to protect hair for DECADES!! :smack:

 

[purecontrol]

If blocking androgen receptors makes things worse, how does one explain Hamilton's often quoted finding that castration can have its beneficial effect on scalp hair for as long as 20-30 years, and quite possibly even longer? While the sharp curtailment of androgen production (castration) isn't exactly the same thing as androgen receptor blockade, it's certainly in the same general neighborhood. You need to explain that, if you're going to use something that happens with prostate cancer cells as an argument not to use antiandrogens to protect scalp hair.

The fact is that no "man" is castrated and that for us we don't want to be. As a result it is not relevant to us since the hormones are completely different ratios.

We are men not women LOL

PS women go bald also ie male pattern baldness and difuse thining.

 

[Bryan]

The fact is that no "man" is castrated and that for us we don't want to be. As a result it is not relevant to us since the hormones are completely different ratios.

We are men not women LOL

PS women go bald also ie male pattern baldness and difuse thining.

I have no idea what your point is, or what it has to do with what's being discussed in this thread.

 

[baldinglikeamofo]

I dont know.....

Blockade causes TOTAL deprivation, which forces the receptor the morph

whereas castration is not total, the 5% testostrone floating around may be enough to keep the receptors from morphing.

 

[cyberprimate]

castration is not total, the 5% testostrone floating around may be enough to keep the receptors from morphing.

Clever answer.

 

[keepinthehair]

Ok, I'll bite.

It is rational to think receptors need to mutate due to inactivity. This in itself is evolution at its best.

However, using an "androgen blocker" such as RU, CB 3-01, Saw Palmettto, Beta Sistosterol etc, simply competes with DHT for the same receptor sites. Ideally, we simply flood the receptors with "dummy" DHT. This dummy molecule only needs to have a small piece of its shape/size/charge affinity similar to DHT to bind to the receptor. The receptor never knows what actually sits there. A good example is Benadryl (diphenhydramine) which is used to block Mast Cell receptors for allergy response. Same concept. Silly little mast cells dont get confused why should the hair follicle.

So, in theory, the hair follicle receptor would be "satisfied" with a dummy DHT like molecule and have no "evolutionary desire" to mutate. Remember to still take finasteride to reduce the ratio of DHT to dummy DHT.

 

[cuebald]

I don't know if I buy that theory- http://www.ncbi.nlm.nih.gov/pubmed/21229554

The link you posted has nothing to do with his post.

 

[Bryan]

I don't know if I buy that theory- http://www.ncbi.nlm.nih.gov/pubmed/21229554

The link you posted has nothing to do with his post.

Unless I posted the wrong link- the link I posted shows that Finasteride upregulates AR's...

I think it's obviously the lack of androgenic stimulation itself (rather than the lack of androgen receptors being stimulated by something) which causes the upregulation of androgen receptors.

 

[keepinthehair]

I think it's obviously the lack of androgenic stimulation itself (rather than the lack of androgen receptors being stimulated by something) which causes the upregulation of androgen receptors.

Well I see your point, but Finasteride does cause an androgen deficiency in terms of DHT....

I believe Bryan is correct, the simple starvation of the receptors causes the follice cell to "panic" and create more receptors. (not mutated).

It would be nice to compare the number of prostate/scalp follicle receptors of castrated/non castrated identical twins. If correct, the castrated male would have the greater number of receptors though not bald (no mutation) while the castrated brother would be bald with fewer receptors.

Unless I am wrong, the study supports the idea of taking AR blocker.

 

[keepinthehair]

I believe Bryan is correct, the simple starvation of the receptors causes the follice cell to "panic" and create more receptors. (not mutated).

It would be nice to compare the number of prostate/scalp follicle receptors of castrated/non castrated identical twins. If correct, the castrated male would have the greater number of receptors though not bald (no mutation) while the noncastrated brother would be bald with fewer receptors.

Unless I am wrong, the study supports the idea of taking AR blocker.

 

[Rabid]

Those scenerios are not particularly relevant to the subject of the thread. In castrates there is no antagonistic androgen receptor activity, so there would be no need to upregulate androgen receptors. The follicle's only response to the unusually low level of agonist activity is to grow and not be miniaturized. In cancer there is abnormal disregulation of upregulation and growth, again not a massive blockade of receptors.

Massive blockade of the receptors is a result of taking powerful anti-androgens internally or rubbing them on the skin. Hair follicles by their nature can "sense" the net effect of total agonist-antagonist activity at their ARs. In certain individuals, when they sense the abnormally high antagonist/agonist ratio from these drugs, the follicles upregulate their ARs accordingly. This would definitely make things worse.

 

[Bryan]

Those scenerios are not particularly relevant to the subject of the thread. In castrates there is no antagonistic androgen receptor activity, so there would be no need to upregulate androgen receptors.

Sure there would be, if what I said previously is correct, and it's a lack of sufficient androgenic stimulation which causes the upregulation of androgen receptors.

 

[Rabid]

Those scenerios are not particularly relevant to the subject of the thread. In castrates there is no antagonistic androgen receptor activity, so there would be no need to upregulate androgen receptors.

Sure there would be, if what I said previously is correct, and it's a lack of sufficient androgenic stimulation which causes the upregulation of androgen receptors.

Low levels of androgen stimulus benefiting hair (as in castrates) while low levels of androgenic stimulus causing upregulation of androgen receptors... How do you reconcile this? Are you saying upregulation may occur in castrates, but with no noticeable consequence? If it's excessive receptor antagonism from anti-androgens on the other hand that leads to upregulation, then both the castrates non-balding and RHA in non-castrates would co-exist.